No recent data are available on hepatitis B virus (HBV) and hepatitis Delta virus (HDV) prevalence in Mauritania. One thousand twenty pregnant women and 946 patients visiting for routine checkups were screened for HBV and HDV infection. Demographic, epidemiological, ethnic, clinical, and biological data were recorded. HBV and HDV genotypes were determined by sequencing and phylogenetic analyses. In the pregnant women and patients cohorts, respectively, the prevalence of HBsAg (10.7% and 18.3%) and anti‐HBcAb (66.3% and 76.5%) indicated high HBV endemicity. In pregnant women, exposure to HBV was significantly associated in multivariate analysis with education level, ethnicity, blood transfusion, and occupation. HDV antibodies (HDVAb) were found in 14.7% of pregnant women. In patients, HBsAg was found less frequently in females than in males. Again in multivariate analysis, exposure to HBV was significantly correlated with gender (males), and HDVAb positivity with age and gender. The HBV DNA viral load was >3 log IU/ml in only 10.1% of pregnant women and in 17.3% of patients. HDV‐RNA was detectable in 21 (67.7%) of the 31 patients positive for HDVAb, and in 11 of the 16 pregnant women positive for HDVAb (68.8%). The most frequent HBV genotypes were: HBV/D, 53%; HBV/E, 35%; and HBV/A, 12%. Sub‐genotyping revealed HBV/D1,/D7, and the recently described/D8. HDV genotypes were: HDV‐1, 90.3% and HDV‐5, 9.7%. This study confirms the high prevalence of HBV and HDV infections in Mauritania and demonstrates the high genetic diversity of HBV in this country. J. Med. Virol. 84: 1186–1198, 2012. © 2012 Wiley Periodicals, Inc.

In Mauritania, HDV co-infection worsens liver disease, both clinically and biologically, as confirmed by the APRI and FibroMeter tests. These tests may be useful for the management of delta hepatitis, which is a major health problem in Mauritania.

Introduction The Gulf Cooperation Council (GCC or 'Arabian Gulf'), comprising Bahrain, Kuwait, Oman, Qatar, Saudi Arabia and United Arab Emirates, is a political organization sharing a common history and culture. All GCC nations have made substantial investments in telecommunications and electronic health infrastructure since 2000. Methods We conducted a literature search in English and Arabic on peer-reviewed e-health research up to December 2014 originating in the GCC. The objective was to retrieve all research on e-health in the GCC and to categorize and analyse it qualitatively to reveal the current state of e-health research and development in the region. Inclusion criteria included peer-reviewed articles, books, book chapters, conference papers and graduate theses written on e-health in the GCC. Blogs, health websites and non-peer-reviewed literature were excluded. Results Three hundred and six articles were retrieved, categorized and analysed qualitatively to reveal the state of e-health research in the GCC. Both country-specific and GCC-wide major themes were identified using NVivo 10.0 qualitative software and summarized. The most common type of study was an overview (35.0%), with common study designs of case studies (26.8%) and descriptive articles (46.4%). Significant themes were: prospective national benefits from e-health, implementation and satisfaction with electronic health records, online technologies in medical education, innovative systems (case studies), and information security and personal health information. Discussion This is the first comprehensive analytical literature review of e-health in the GCC. Important research gaps were identified: few cost-benefit analyses, controlled interventional studies, or research targeting gender and religious issues were retrieved.

Chronic obstructive pulmonary disease (COPD), associated with cigarette smoke-induced (CS-induced) emphysema, contributes significantly to the global health care burden of disease. Although chronic kidney disease (CKD) may occur in patients with COPD, the relationship between COPD and CKD remains unclear. Using a murine model of experimental COPD, we show that chronic CS exposure resulted in marked kidney injury and fibrosis, as evidenced by histological and ultrastructural changes, altered macrophage subpopulations, and expression of tissue injury, fibrosis, and oxidative stress markers. CS induced mitochondrial dysfunction, and increased autophagic flux in kidney tissues and in kidney tubular epithelial (HK-2) cells, as determined by LC3B turnover assays. Mice heterozygous for Beclin-1 (Becn1+/-) were protected from the development of kidney tissue injury and renal fibrosis in response to CS exposure, and displayed impaired basal and inducible mitochondrial turnover by mitophagy. Interestingly, CS caused a reduction of Beclin-1 expression in mouse kidneys and kidney tubular epithelial cells, attributed to increased autophagy-dependent turnover of Beclin-1. These results suggest that Beclin-1 is required for CS-induced kidney injury and that reduced levels of Beclin-1 may confer renoprotection. These results identify the kidney as a target for CS-induced injury in COPD and the Beclin-1-dependent autophagy pathway as a potential therapeutic target in CKD.

No abstract